scholarly journals Developmental programming of the metabolic syndrome by maternal nutritional imbalance: how strong is the evidence from experimental models in mammals?

2004 ◽  
Vol 561 (2) ◽  
pp. 355-377 ◽  
Author(s):  
James A. Armitage ◽  
Imran Y. Khan ◽  
Paul D. Taylor ◽  
Peter W. Nathanielsz ◽  
Lucilla Poston
Keyword(s):  
Metabolic Syndrome ◽  
Developmental Programming ◽  
Experimental Models ◽  
The Metabolic Syndrome ◽  
Nutritional Imbalance

scholarly journals Developmental Programming of the Metabolic Syndrome: Can We Reprogram with Resveratrol?

2018 ◽  
Vol 19 (9) ◽  
pp. 2584 ◽  
Author(s):  
You-Lin Tain ◽  
Chien-Ning Hsu
Keyword(s):  
Metabolic Syndrome ◽  
Early Life ◽  
Wide Spectrum ◽  
Molecular Targets ◽  
Developmental Programming ◽  
Developmental Origins ◽  
Polyphenolic Compound ◽  
Beneficial Effects ◽  
The Metabolic Syndrome ◽  
Health And Disease

Metabolic syndrome (MetS) is a mounting epidemic worldwide. MetS can start in early life, in a microenvironment that is now known as the developmental origins of health and disease (DOHaD). The concept of DOHaD also offers opportunities for reprogramming strategies that aim to reverse programming processes in early life. Resveratrol, a polyphenolic compound has a wide spectrum of beneficial effects on human health. In this review, we first summarize the epidemiological and experimental evidence supporting the developmental programming of MetS. This review also presents an overview of the evidence linking different molecular targets of resveratrol to developmental programming of MetS-related disorders. This will be followed by studies documenting resveratrol as a reprogramming agent to protect against MetS-related disorders. Further clinical studies are required in order to bridge the gap between animal models and clinical trials in order to establish the effective dose and therapeutic duration for resveratrol as a reprogramming therapy on MetS disorders from developmental origins.

scholarly journals Experimental rat models to study the metabolic syndrome

2009 ◽  
Vol 102 (9) ◽  
pp. 1246-1253 ◽  
Author(s):  
Amaya Aleixandre de Artiñano ◽  
Marta Miguel Castro
Keyword(s):  
Diabetes Mellitus ◽  
Metabolic Syndrome ◽  
Experimental Model ◽  
Insulin Dependent Diabetes Mellitus ◽  
Experimental Models ◽  
Zucker Rats ◽  
Dependent Diabetes Mellitus ◽  
The Metabolic Syndrome ◽  
Insulin Dependent ◽  
Obese Zucker Rats

Being the metabolic syndrome a multifactorial condition, it is difficult to find adequate experimental models to study this pathology. The obese Zucker rats, which are homozygous for the fa allele, present abnormalities similar to those seen in human metabolic syndrome and are a widely extended model of insulin resistance. The usefulness of these rats as a model of non-insulin-dependent diabetes mellitus is nevertheless questionable, and they neither can be considered a clear experimental model of hypertension. Some experimental models different from the obese Zucker rats have also been used to study the metabolic syndrome. Some derive from the spontaneously hypertensive rats (SHR). In this context, the most important are the obese SHR, usually named Koletsky rats. Hyperinsulinism, associated with either normal or slightly elevated levels of blood glucose, is present in these animals, but SHR/N-corpulent rats are a more appropriated model of non-insulin-dependent diabetes mellitus. The SHR/NDmc corpulent rats, a subline of SHR/N-corpulent rats, also exhibit metabolic and histopathologic characteristics associated with human metabolic disorders. A new animal model of the metabolic syndrome, stroke-prone–SHR (SHRSP) fatty rats, was obtained by introducing a segment of the mutant leptin receptor gene from the Zucker line heterozygous for the fa gene mutation into the genetic background of the SHRSP. Very recently, it has been developed as a non-obese rat model with hypertension, fatty liver and characteristics of the metabolic syndrome by transgenic overexpression of a sterol-regulatory element-binding protein in the SHR rats. The Wistar Ottawa Karlsburg W rats are also a new strain that develops a nearly complete metabolic syndrome. Moreover, a new experimental model of low-capacity runner rats has also been developed with elevated blood pressure levels together with the other hallmarks of the metabolic syndrome.

scholarly journals Cardiac Autonomic Neuropathy: A Progressive Consequence of Chronic Low-Grade Inflammation in Type 2 Diabetes and Related Metabolic Disorders

2020 ◽  
Vol 21 (23) ◽  
pp. 9005
Author(s):  
Nour-Mounira Z. Bakkar ◽  
Haneen S. Dwaib ◽  
Souha Fares ◽  
Ali H. Eid ◽  
Yusra Al-Dhaheri ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Autonomic Neuropathy ◽  
Experimental Models ◽  
Cardiac Autonomic Neuropathy ◽  
Low Grade ◽  
Metabolic Inflammation ◽  
The Metabolic Syndrome ◽  
Cardiovascular Morbidity And Mortality

Cardiac autonomic neuropathy (CAN) is one of the earliest complications of type 2 diabetes (T2D), presenting a silent cause of cardiovascular morbidity and mortality. Recent research relates the pathogenesis of cardiovascular disease in T2D to an ensuing chronic, low-grade proinflammatory and pro-oxidative environment, being the hallmark of the metabolic syndrome. Metabolic inflammation emerges as adipose tissue inflammatory changes extending systemically, on the advent of hyperglycemia, to reach central regions of the brain. In light of changes in glucose and insulin homeostasis, dysbiosis or alteration of the gut microbiome (GM) emerges, further contributing to inflammatory processes through increased gut and blood–brain barrier permeability. Interestingly, studies reveal that the determinants of oxidative stress and inflammation progression exist at the crossroad of CAN manifestations, dictating their evolution along the natural course of T2D development. Indeed, sympathetic and parasympathetic deterioration was shown to correlate with markers of adipose, vascular, and systemic inflammation. Additionally, evidence points out that dysbiosis could promote a sympatho-excitatory state through differentially affecting the secretion of hormones and neuromodulators, such as norepinephrine, serotonin, and γ-aminobutyric acid, and acting along the renin–angiotensin–aldosterone axis. Emerging neuronal inflammation and concomitant autophagic defects in brainstem nuclei were described as possible underlying mechanisms of CAN in experimental models of metabolic syndrome and T2D. Drugs with anti-inflammatory characteristics provide potential avenues for targeting pathways involved in CAN initiation and progression. The aim of this review is to delineate the etiology of CAN in the context of a metabolic disorder characterized by elevated oxidative and inflammatory load.

scholarly journals ZBTB16 and Metabolic Syndrome: a Network Perspective

2017 ◽  
pp. S357-S365 ◽  
Author(s):  
O. ŠEDA ◽  
L. ŠEDOVÁ ◽  
J. VČELÁK ◽  
M. VAŇKOVÁ ◽  
F. LIŠKA ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Association Studies ◽  
Experimental Models ◽  
Current Evidence ◽  
Lipid Levels ◽  
Genetic Determinants ◽  
Btb Domain ◽  
The Metabolic Syndrome ◽  
Metabolic Syndrome Components ◽  
Candidate Node

Metabolic syndrome is a prevalent, complex condition. The search for genetic determinants of the syndrome is currently undergoing a paradigm enhancement by adding systems genetics approaches to association studies. We summarize the current evidence on relations between an emergent new candidate, zinc finger and BTB domain containing 16 (ZBTB16) transcription factor and the major components constituting the metabolic syndrome. Information stemming from studies on experimental models with altered Zbtb16 expression clearly shows its effect on adipogenesis, cardiac hypertrophy and fibrosis, lipid levels and insulin sensitivity. Based on current evidence, we provide a network view of relations between ZBTB16 and hallmarks of metabolic syndrome in order to elucidate the potential functional links involving the ZBTB16 node. Many of the identified genes interconnecting ZBTB16 with all or most metabolic syndrome components are linked to immune function, inflammation or oxidative stress. In summary, ZBTB16 represents a promising pleiotropic candidate node for metabolic syndrome.

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